Brockmann, Knut

[["dc.bibliographiccitation.firstpage","39"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Gastroenterology"],["dc.bibliographiccitation.lastpage","48"],["dc.bibliographiccitation.volume","42"],["dc.contributor.author","Gerstner, Thorsten"],["dc.contributor.author","Buesing, Deike"],["dc.contributor.author","Bell, Nellie"],["dc.contributor.author","Longin, Elke"],["dc.contributor.author","Kasper, Johannes-Martin"],["dc.contributor.author","Klostermann, Wolfgang"],["dc.contributor.author","Hebing, Burkhard"],["dc.contributor.author","Hanefeld, Folker"],["dc.contributor.author","Eckel, Ulrich"],["dc.contributor.author","Hoffmann, Reiner"],["dc.contributor.author","Bettendorf, Ulrich"],["dc.contributor.author","Weidner, Birgit"],["dc.contributor.author","Wiemer-Kruel, Adelheid"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Neumann, Fritz-Wilhelm"],["dc.contributor.author","Sandrieser, Thorsten"],["dc.contributor.author","Wolff, Markus"],["dc.contributor.author","Koenig, Stephan"],["dc.date.accessioned","2018-11-07T11:06:51Z"],["dc.date.available","2018-11-07T11:06:51Z"],["dc.date.issued","2007"],["dc.description.abstract","Background Acute pancreatitis is rarely seen in children, and, in contrast to cases in adults, it is often drug induced. One possible medication is the antiepileptic drug valproic acid (VPA), which is commonly prescribed for generalized and focal epilepsy, migraine, neuropathic pain, and bipolar disorder. The common side effects associated with VPA are typically benign, but less common but more serious adverse effects may occur. These include hepatotoxicity, hyperammonemic encephalopathy, coagulation disorders, and pancreatitis. Since 1979, a few cases of pancreatitis induced by VPA have been published in the medical literature. Methods We mailed a questionnaire to all members of the \"German Section of the International League against Epilepsy,\" asking about VPA-induced side effects. We also reviewed the medical literature for VPA-induced pancreatitis. Results Fifty-three publications (90 patients) published from 1979 to 2005 were found. Our survey in Germany, however, yielded 16 cases of pancreatitis from 1994 to 2003 whose original files we could study in detail. None of these patients had been published previously. Conclusion The difference between 90 patients reported worldwide from 1979 to 2005 and the 16 new documented cases from only Germany over 10 years corroborates that the occurrence of this severe side effect is under reported."],["dc.identifier.doi","10.1007/s00535-006-1961-4"],["dc.identifier.isi","000244483900005"],["dc.identifier.pmid","17322992"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52417"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Tokyo"],["dc.relation.issn","0944-1174"],["dc.title","Valproic acid-induced pancreatitis: 16 new cases and a review of the literature"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","701"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","706"],["dc.bibliographiccitation.volume","65"],["dc.contributor.author","Hanefeld, Folker"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Pouwels, Petra J. W."],["dc.contributor.author","Wilken, Barbara"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Dechent, Peter"],["dc.date.accessioned","2018-11-07T10:55:47Z"],["dc.date.available","2018-11-07T10:55:47Z"],["dc.date.issued","2005"],["dc.description.abstract","Background: Pelizaeus-Merzbacher disease (PMD) is a rare X-linked recessive neurologic disorder caused by a mutation in the proteolipid protein (PLP) gene on chromosome Xq22. The associated depletion of PLP and severe reduction of other major myelin proteins results in dysmyelination. MRI reveals loss of T1 contrast between gray and affected white matter and T2 hyperintensities of white matter due to elevated water content. Methods: In vivo proton magnetic resonance spectroscopy (MRS) was used to determine cerebral metabolite patterns in five patients with genetically proven PMD. Absolute metabolite concentrations were obtained in cortical gray matter, affected white matter, and basal ganglia and compared to age-matched control values. Results: In comparison to age-matched controls, MRS of affected white matter resembled the metabolite pattern of cortical gray matter, as indicated by increased concentrations of N-acetylaspartate and N-acetylaspartylglutamate (tNAA), glutamine (Gln), myo-inositol ( Ins), and creatine and phosphocreatine. Most remarkably, the concentration of choline-containing compounds was reduced. Parietal gray matter and basal ganglia appeared normal but showed a tendency for elevated tNAA, Gln, and Ins. Conclusions: Magnetic resonance spectroscopy (MRS)-detected alterations are consistent with enhanced neuroaxonal density, astrogliosis, and reduction of oligodendroglia. These disturbances in cellular composition are in close agreement with the histopathologic features characteristic of dys- and hypomyelination. The proton MRS profile of Pelizaeus-Merzbacher disease (PMD) differs from the pattern commonly observed in demyelinating disorders and allows PMD to be distinguished from other leukodystrophies."],["dc.identifier.doi","10.1212/01.wnl.0000174642.32187.20"],["dc.identifier.isi","000231821300009"],["dc.identifier.pmid","16157902"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49865"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0028-3878"],["dc.title","Quantitative proton MRS of Pelizaeus-Merzbacher disease - Evidence of dys- and hypomyelination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","165"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neuropediatrics"],["dc.bibliographiccitation.lastpage","166"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Hanefeld, Folker"],["dc.date.accessioned","2018-11-07T09:02:00Z"],["dc.date.available","2018-11-07T09:02:00Z"],["dc.date.issued","2001"],["dc.identifier.doi","10.1055/s-2001-16617"],["dc.identifier.isi","000170536500011"],["dc.identifier.pmid","11521216"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24569"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0174-304X"],["dc.title","Progressive elevation of liver enzymes in a child treated with sulthiame"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","236"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Pediatric Neurology"],["dc.bibliographiccitation.lastpage","238"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Rostasy, Kevin"],["dc.contributor.author","Diepold, K."],["dc.contributor.author","Buckard, Johannes A."],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Wilken, Barbara"],["dc.contributor.author","Hanefeld, Folker"],["dc.date.accessioned","2018-11-07T10:36:44Z"],["dc.date.available","2018-11-07T10:36:44Z"],["dc.date.issued","2003"],["dc.description.abstract","Corticosteroids and intravenous immunoglobulins belong to the first line of treatment in chronic inflammatory demyelinating polyneuropathy. In patients with a progressive course, plasma exchange and immunomodulatory drugs are added to the regimen. To reduce the side effects of long-term oral prednisolone, high-dose pulsatile intravenous methylprednisolone treatment has been advocated. We report two children with chronic inflammatory demyelinating polyneuropathy who, after high-dose intravenous pulsatile methylprednisolone, experienced a significant clinical deterioration with profound loss of muscle strength. Both patients improved after changing treatment to immunoglobulins in one and cyclosporine combined with immunoglobulins and oral prednisolone in the other. (C) 2003 by Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/S0887-8994(03)00222-4"],["dc.identifier.isi","000186872100009"],["dc.identifier.pmid","14629908"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45395"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0887-8994"],["dc.title","Progressive muscle weakness after high-dose steroids in two children with CIDP"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","663"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","666"],["dc.bibliographiccitation.volume","252"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Dumitrescu, A. M."],["dc.contributor.author","Best, T. T."],["dc.contributor.author","Hanefeld, Folker"],["dc.contributor.author","Refetoff, S."],["dc.date.accessioned","2018-11-07T10:51:38Z"],["dc.date.available","2018-11-07T10:51:38Z"],["dc.date.issued","2005"],["dc.description.abstract","We previously reported two unrelated boys aged 3 and 8 years with mutations in the thyroid hormone transporter gene MCT8 resulting in severe global retardation and an uncommon pattern of thyroid hormone abnormalities. We now further describe an unusual neurological phenotype associated with these mutations, namely paroxysmal kinesigenic dyskinesias (PKD), provoked by certain stimuli including changing of their clothes or diapers. It is not clear how the MCT8 defect causes PKDs. PKDs have been previously noted in patients with thyroid abnormalities. This novel X-linked condition widens the spectrum of secondary PKDs."],["dc.description.sponsorship","NCRR NIH HHS [RR 00055]; NIDDK NIH HHS [DK 15070]"],["dc.identifier.doi","10.1007/s00415-005-0713-3"],["dc.identifier.isi","230033000005"],["dc.identifier.pmid","15834651"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48934"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.title","X-linked paroxysmal dyskinesia and severe global retardation caused by defective MCT8 gene"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","38"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","46"],["dc.bibliographiccitation.volume","52"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Bjornstad, A."],["dc.contributor.author","Dechent, Peter"],["dc.contributor.author","Korenke, C. G."],["dc.contributor.author","Smeitink, J."],["dc.contributor.author","Trijbels, JMF"],["dc.contributor.author","Athanassopoulos, S."],["dc.contributor.author","Villagran, R."],["dc.contributor.author","Skjeldal, O. H."],["dc.contributor.author","Wilichowski, E."],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Hanefeld, Folker"],["dc.date.accessioned","2018-11-07T10:19:26Z"],["dc.date.available","2018-11-07T10:19:26Z"],["dc.date.issued","2002"],["dc.description.abstract","A deficiency of succinate dehydrogenase is a rare cause of mitochondrial encephalomyopathy. Three patients, 2 sisters and I boy from an unrelated family, presented with symptoms and magnetic resonance imaging signs of leukoencephalopathy. Localized proton magnetic resonance spectroscopy indicated a prominent singlet at 2.40ppm in cerebral and cerebellar white matter not present in gray matter or basal ganglia. The signal was also elevated in cerebrospinal fluid and could be identified as originating from the two equivalent methylene groups of succinate. Subsequently, an isolated deficiency of complex II (succinate:ubiquinone oxidoreductase) was demonstrated in 2 patients in muscle and fibroblasts. One of the sisters died at the age of 18 months. Postmortem examination showed the neuropathological characteristics of Leigh syndrome. Her younger sister, now 12 months old, is also severely affected; the boy, now 6 years old, follows a Milder, fluctuating clinical course. Magnetic resonance spectroscopy provides a characteristic pattern in succinate dehydrogenase deficiency."],["dc.identifier.doi","10.1002/ana.10232"],["dc.identifier.isi","000176451800007"],["dc.identifier.pmid","12112045"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41656"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0364-5134"],["dc.title","Succinate in dystrophic white matter: A proton magnetic resonance spectroscopy finding characteristic for complex II deficiency"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","45"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Brain and Development"],["dc.bibliographiccitation.lastpage","50"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Pouwels, Petra J.W."],["dc.contributor.author","Dechent, Peter"],["dc.contributor.author","Flanigan, Kevin M."],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Hanefeld, Folker"],["dc.date.accessioned","2021-06-01T10:50:17Z"],["dc.date.available","2021-06-01T10:50:17Z"],["dc.date.issued","2003"],["dc.description.abstract","Magnetic resonance imaging of a girl with giant axonal neuropathy revealed a progressive white matter disease. In close agreement with histopathological features reported previously, localized proton magnetic resonance spectroscopy at 9 and 12 years of age indicated a specific damage or loss of axons (reduced N-acetylaspartate and N-acetylaspartylglutamate) accompanied by acute demyelination (elevated choline-containing compounds, myo-inositol, and lactate) in white matter as well as a generalized proliferation of glial cells (elevated choline-containing compounds and myo-inositol) in both gray and white matter. (C) 2002 Elsevier Science B.V. All rights reserved."],["dc.identifier.doi","10.1016/s0387-7604(02)00154-7"],["dc.identifier.isi","000180767900008"],["dc.identifier.pmid","12536033"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86597"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0387-7604"],["dc.title","Cerebral proton magnetic resonance spectroscopy of a patient with giant axonal neuropathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","335"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Neuropediatrics"],["dc.bibliographiccitation.lastpage","336"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Bönnemann, C. G."],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Hanefeld, Folker"],["dc.date.accessioned","2018-11-07T10:34:30Z"],["dc.date.available","2018-11-07T10:34:30Z"],["dc.date.issued","2003"],["dc.identifier.isi","000188084300012"],["dc.identifier.pmid","14681763"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44889"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0174-304X"],["dc.title","Muscle ultrasound in Bethlem myopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","528"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","European Journal of Pediatrics"],["dc.bibliographiccitation.lastpage","530"],["dc.bibliographiccitation.volume","161"],["dc.contributor.author","Huppke, Peter"],["dc.contributor.author","Wilken, Barbara"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Sattler, B."],["dc.contributor.author","Hanefeld, Folker"],["dc.date.accessioned","2018-11-07T09:58:54Z"],["dc.date.available","2018-11-07T09:58:54Z"],["dc.date.issued","2002"],["dc.description.abstract","We report on an 11-year-old girl who developed multiple joint contractures over a period of 3 months. The disease presented with progressive involvement of the fingers, elbows, shoulders, knees and feet and was not accompanied by other symptoms. Laboratory investigations showed eosinophilia and hypergammaglobulinaemia. Muscle ultrasound and magnetic resonance imaging of the right forearm revealed thickened fascia and a full thickness biopsy confirmed the diagnosis of eosinophilic fasciitis. Following treatment with pulsed steroids, the contractures resolved. Conclusion: our case shows that eosinophilic fasciitis can present without skin involvement and arthritis and therefore has to be regarded as a differential diagnosis of contractures in childhood. Pulsed steroid treatment was effective and without side-effects."],["dc.identifier.doi","10.1007/s00431-002-1038-1"],["dc.identifier.isi","000178831300004"],["dc.identifier.pmid","12297898"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37469"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0340-6199"],["dc.title","Eosinophilic fasciitis leading to painless contractures"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","476"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","485"],["dc.bibliographiccitation.volume","50"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Wang, D."],["dc.contributor.author","Korenke, C. G."],["dc.contributor.author","von Moers, A."],["dc.contributor.author","Ho, Y. Y."],["dc.contributor.author","Pascual, J. M."],["dc.contributor.author","Kuang, K."],["dc.contributor.author","Yang, H."],["dc.contributor.author","Ma, L."],["dc.contributor.author","Kranz-Eble, P."],["dc.contributor.author","Fischbarg, J."],["dc.contributor.author","Hanefeld, Folker"],["dc.contributor.author","De Vivo, D. C."],["dc.date.accessioned","2018-11-07T08:33:30Z"],["dc.date.available","2018-11-07T08:33:30Z"],["dc.date.issued","2001"],["dc.description.abstract","Glut-l deficiency syndrome was first described in 1991 as a sporadic clinical condition, later shown to be the result of haploinsufficiency. We now report a family with Glut-l deficiency syndrome affecting 5 members over 3 generations. The syndrome behaves as an autosomal dominant condition. Affected family members manifested mild to severe seizures, developmental delay, ataxia, hypoglycorrhachia, and decreased erythrocyte 3-O-methyl-D-glucose uptake. Seizure frequency and severity were aggravated by fasting, and responded to a carbohydrate load. Glut-1 immunoreactivity in erythrocyte membranes was normal. A heterozygous R126H missense mutation was identified in the 3 patients available for testing, 2 brothers (Generation 3) and their mother (Generation 2). The sister and her father were clinically and genotypically normal. In vitro mutagenesis studies in Xenopus laevis oocytes demonstrated significant decreases in the transport of 3-O-methyl-D-glucose and dehydroascorbic acid. Xenopus oocyte membranes expressed high amounts of the R126H mutant Glut-1. Kinetic analysis indicated that replacement of arginine-126 by histidine in the mutant Glut-l resulted in a lower V-max. These studies demonstrate the pathogenicity of the R126H missense mutation and transmission of Glut-1 deficiency syndrome as an autosomal dominant trait."],["dc.identifier.doi","10.1002/ana.1222"],["dc.identifier.isi","000171402200009"],["dc.identifier.pmid","11603379"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17590"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0364-5134"],["dc.title","Autosomal dominant Glut-1 deficiency syndrome and familial epilepsy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]